PI3 kinase inhibition improves vascular malformations in mouse models of hereditary haemorrhagic telangiectasia
Ola R, Dubrac A, Han J, Zhang F, Fang JS, Larrivée B, Lee M, Urarte AA, Kraehling JR, Genet G, Hirschi KK, Sessa WC, Canals FV, Graupera M, Yan M, Young LH, Oh PS, Eichmann A. PI3 kinase inhibition improves vascular malformations in mouse models of hereditary haemorrhagic telangiectasia. Nature Communications 2016, 7: 13650. PMID: 27897192, PMCID: PMC5141347, DOI: 10.1038/ncomms13650.Peer-Reviewed Original ResearchMeSH KeywordsActivin Receptors, Type IActivin Receptors, Type IIAnimalsBone Morphogenetic ProteinsDisease Models, AnimalGene DeletionHuman Umbilical Vein Endothelial CellsHumansMiceModels, BiologicalNeovascularization, PathologicPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsRetinaSignal TransductionTelangiectasia, Hereditary HemorrhagicVascular Endothelial Growth Factor Receptor-2Vascular MalformationsConceptsHereditary haemorrhagic telangiectasia type 2Activin receptor-like kinase 1Arteriovenous malformationsAVM formationAlk1 deletionPharmacological PI3K inhibitionExcessive angiogenesisSerine-threonine kinase receptorsBone morphogenetic protein 9PI3K pathway activationHereditary haemorrhagic telangiectasiaPI3-kinase inhibitionReceptor-like kinase 1PI3K/AktPI3K inhibitionVascular lesionsVascular malformationsGastrointestinal tractMouse modelProtein 9Type 2Kinase 1Retinal vesselsGenetic deletionALK1 genemiR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart
Li N, Hwangbo C, Jaba IM, Zhang J, Papangeli I, Han J, Mikush N, Larrivée B, Eichmann A, Chun HJ, Young LH, Tirziu D. miR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart. Scientific Reports 2016, 6: 21228. PMID: 26888314, PMCID: PMC4758045, DOI: 10.1038/srep21228.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCardiomegalyEndotheliumMechanistic Target of Rapamycin Complex 1Membrane ProteinsMiceMice, KnockoutMicroRNAsMultiprotein ComplexesMyocytes, CardiacNeovascularization, PathologicNitric OxideNitric Oxide Synthase Type IIIProteinsProto-Oncogene Proteins c-aktRGS ProteinsTOR Serine-Threonine KinasesUp-RegulationConceptsHypertrophic responseMiR-182Myocardial hypertrophyEndothelial-cardiomyocyte crosstalkLV pressure overloadEndothelium-derived NOPlacental growth factorMyocardial hypertrophic responseDevelopment of hypertrophyDegradation of regulatorsMiR-182 targetsHemodynamic demandsPressure overloadPlGF expressionBlood supplyParacrine actionCardiomyocyte hypertrophyMyocardial angiogenesisCardiac angiogenesisTreatment inhibitsHypertrophyAKT/mTORC1 pathwaysNovel targetAkt/Growth factor